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Exercise during pregnancy attenuates prenatal high‐fat diet‐induced hypermethylation of Pgc‐1α in skeletal muscle
Author(s) -
Laker Rhianna Che,
Lillard Travis,
Okutsu Mitsuhara,
Connelly Jessica J,
Yan Zhen
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1086.19
Subject(s) - offspring , endocrinology , dna methylation , medicine , epigenetics , pregnancy , skeletal muscle , fetus , methylation , obesity , cpg site , biology , gene expression , genetics , gene
Maternal obesity predisposes the fetus to later metabolic disease. We determined whether maternal diet and exercise impose epigenetic influences in offspring on a metabolic master regulator, peroxisome proliferator activated receptor γ co‐activator 1α (Pgc‐1α). Female C57BL6 mice were exposed to the following environments for 6 wks prior to, and throughout pregnancy: sedentary with normal chow, sedentary with high‐fat diet (HFD), or exercise with HFD. Genomic DNA from skeletal muscle and liver were isolated from neonatal mice for DNA methylation analysis of the Pgc‐1α promoter using pyro‐sequencing. There were no differences between groups in litter size or offspring weight. Pgc‐1α methylation of CpG −260 was increased (P<0.05) in offspring skeletal muscle when exposed to maternal HFD. Maternal exercise attenuated this HFD‐induced hypermethylation. Neither HFD nor exercise effected Pgc‐1α methylation in the liver of the offspring. In conclusion, maternal HFD results in neonatal, muscle specific hypermethylation of Pgc‐1α at a site associated with metabolic disease in humans. This epigenetic event was suppressed by manipulation of the gestational environment through maternal exercise. These tissue‐specific epigenetic modifications may have important consequences for later health and disease.